The Role of Cyclooxygenase-2 in Cell Proliferation and Cell Death in Human MalignanciesReport as inadecuate

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International Journal of Cell BiologyVolume 2010 2010, Article ID 215158, 21 pages

Review Article

Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, 9 rue Edward Steichen, 2540 Luxembourg, Luxembourg

Dipartimento di Biologia, Università di Roma di Roma Tor Vergata, Via Ricerca Scientifica snc, 00133 Rome, Italy

Received 16 July 2009; Accepted 18 December 2009

Academic Editor: Simone Fulda

Copyright © 2010 Cyril Sobolewski et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It is well admitted that the link between chronic inflammation and cancer involves cytokines and mediators of inflammatory pathways, which act during the different steps of tumorigenesis. The cyclooxygenases COXs are a family of enzymes, which catalyze the rate-limiting step of prostaglandin biosynthesis. This family contains three members: ubiquitously expressed COX-1, which is involved in homeostasis; the inducible COX-2 isoform, which is upregulated during both inflammation and cancer; and COX-3, expressed in brain and spinal cord, whose functions remain to be elucidated. COX-2 was described to modulate cell proliferation and apoptosis mainly in solid tumors, that is, colorectal, breast, and prostate cancers, and, more recently, in hematological malignancies. These findings prompt us to analyze here the effects of a combination of COX-2 inhibitors together with different clinically used therapeutic strategies in order to further improve the efficiency of future anticancer treatments. COX-2 modulation is a promising field investigated by many research groups.

Author: Cyril Sobolewski, Claudia Cerella, Mario Dicato, Lina Ghibelli, and Marc Diederich



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